Furthermore, our assumption that the association between whole blood AKAP7 levels and post-stroke BBB disruption is driven by a lymphocyte-dependent mechanism was based on the observation of lymphocyte-specific AKAP7 expression on isolated leukocyte subpopulations; however, this analysis was restricted to a limited number of healthy individuals and only surveyed the three most predominant subpopulations of leukocytes. This evidence concerns the gene AKAP7 and stroke disorder.